Jilka R L, Cohn D V
Endocrinology. 1983 Mar;112(3):945-50. doi: 10.1210/endo-112-3-945.
Stimulators of bone resorption, such as PTH, 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], or prostaglandin E2 (PGE2), do not cause calcium release from cultured calvaria of the genetically determined osteopetrotic microphthalmic (mi/ mi) mouse, due to a defect in the function of osteoclasts. To investigate the capacity of cells of mi/mi bone to degrade collagen, calvaria of 1- to 3-day-old normal and mi/mi littermates were labeled in vivo with [3H]proline 16 h before removal, followed by culture in resorption medium. PTH, 1,25-(OH)2D3, and PGE2 stimulated the release of 3H-labeled material into the culture medium from both normal and mi/mi calvaria. The labeled substance released was of collagenous origin, as indicated by its content of hydroxyproline and susceptibility to collagenase. PTH also stimulated the release of 3H-labeled materials from normal calvaria labeled in vivo 112 h before the mice were killed, but had little or no effect on 3H release from the mi/mi bone, indicating that only noncalcified collagen is susceptible to hormone-stimulated degradation in osteopetrotic bone. We conclude that a portion of the hormone-stimulated resorptive mechanism, namely collagenolysis, is functional in bone of mi/mi mice. This result helps to pinpoint the resorptive defect in mi/ mi bone to a failure to dissolve mineral, rather than a more general phenomenon of failure to remove both mineral and matrix.
骨吸收刺激因子，如甲状旁腺激素（PTH）、1,25 - 二羟胆钙化醇[1,25-(OH)₂D₃]或前列腺素E₂（PGE₂），不会导致基因决定的骨质石化性小眼（mi/mi）小鼠培养颅骨释放钙，这是由于破骨细胞功能缺陷所致。为了研究mi/mi小鼠骨细胞降解胶原蛋白的能力，在处死前16小时，给1至3日龄正常和mi/mi同窝小鼠的颅骨在体内用[³H]脯氨酸标记，随后在吸收培养基中培养。PTH、1,25-(OH)₂D₃和PGE₂刺激正常和mi/mi小鼠颅骨释放³H标记物到培养基中。释放的标记物质来源于胶原蛋白，这可通过其羟脯氨酸含量和对胶原酶的敏感性来表明。PTH还刺激在处死小鼠前112小时在体内标记的正常小鼠颅骨释放³H标记物，但对mi/mi小鼠骨的³H释放几乎没有影响，这表明在骨质石化性骨中只有未钙化的胶原蛋白易受激素刺激的降解作用。我们得出结论，激素刺激的吸收机制的一部分，即胶原溶解，在mi/mi小鼠的骨中是有功能的。这一结果有助于将mi/mi小鼠骨的吸收缺陷定位到矿物质溶解失败，而不是更普遍的矿物质和基质去除失败的现象。
